02161naa a2200253 a 450000100080000000500110000800800410001902400350006010000190009524501570011426000090027152013970028065000110167765000170168865300190170570000170172470000190174170000170176070000140177770000290179170000180182070000160183877300530185413055122015-02-25       2009    bl uuuu     u00u1 u    #d7 a10.1007/s11295-008-0191-82DOI1 aSZANKOWSKI, I.  aHighly scab-resistant transgenic aplle lines achieved by introgression of HcrVf2 controlled by different native promoter lengths.h[electronic resource]  c2009  aApple scab, caused by the ascomycete Venturia inaequalis, is the most damaging fungal disease of commercial apple orchards. Functional scab resistance genes are present in some wild Malus species. The HcrVf2 gene, derived from the Vf-region of the wild apple Malus floribunda 821 and encoding a receptor-like protein, has proved to confer scab resistance in a transgenic susceptible cultivar. In order to minimize nonplant DNA in genetically modified apple and to go a step toward the development of cisgenic apples, we have studied the capability of the HcrVf2 gene to confer apple scab resistance when it is controlled by its own promoter. Three promoter deletion constructs containing 115, 288, and 779 bp of the 5? untranslated region and the HcrVf2 gene were used to transform the scab susceptible apple cvs. ‘Gala’ and ‘Elstar.’ The influence of the promoter length on both the HcrVf2 expression level and the response to V. inaequalis was analyzed in different transgenic lines. Promoter length was found to influence both the constitutive transcription levels of HcrVf2 in transgenic lines and the resistance level. Highly scab resistant ‘Elstar’ and ‘Gala’ plants were obtained, proving that the HcrVf2 gene controlled by its native promoter is effective in conferring resistance to V. inaequalis similarly as Vf introgressed in apple cvs. through classical breeding.  aMaçã  aResistência  aMalus venturia1 aWAISMANN, S.1 aDEGENHARDT, J.1 aPATOCCHI, A.1 aPARIS, R.1 aSILFVERBERG-DILWORTH, E.1 aBROGGIANI, G.1 aGESSLER, C.  tTree Genetics & Genomesgv. 5, p. 349-358, 2009.